Patrick A Calvert1, James Cockburn1, Dylan Wynne1, Peter Ludman1, Bushra S Rana1, David Northridge1, Michael J Mullen1, Iqbal Malik1, Mark Turner1, Saib Khogali1, Gruschen R Veldtman1, Martin Been1, Rob Butler1, John Thomson1, Jonathan Byrne1, Philip MacCarthy1, Lindsay Morrison1, Len M Shapiro1, Ben Bridgewater1, Jo de Giovanni1, David Hildick-Smith2. 1. From the University Hospitals Birmingham National Health Service Foundation Trust, Birmingham, UK (P.A.C., P.L., J.d.G.); University of Cambridge, Cambridge, UK (P.A.C.); Papworth Hospital National Health Service Foundation Trust, Cambridge, UK (P.A.C., B.S.R., L.M.S.); Sussex Cardiac Centre, Brighton and Sussex University Hospitals, Brighton, UK (J.C., D.W., D.H.-S.); Edinburgh Royal Infirmary, Edinburgh, UK (D.N.); The Heart Hospital, University College London, London, UK (M.J.M.); Imperial College Healthcare National Health Service Trust, London, UK (I.M.); University Hospitals Bristol National Health Service Foundation Trust, Bristol, UK (M.T.); Heart and Lung Centre, New Cross Hospital, Wolverhampton, UK (S.K.); University Hospital Southampton National Health Service Foundation Trust, Southampton, UK (G.R.V.); Walsgrave Hospital Coventry, Coventry, UK (M.B.); University Hospital North Staffordshire National Health Service Trust, Stoke-on-Trent, UK (R.B.); Leeds Teaching Hospitals National Health Service Trust, Leeds, UK (J.T.); King's College Hospital National Health Service Foundation Trust, London, UK (J.B., P.M.); Liverpool Heart and Chest Hospitals National Health Service Foundation Trust, Liverpool, UK (L.M.); and University Hospital of South Manchester, Manchester, UK (B.B.). 2. From the University Hospitals Birmingham National Health Service Foundation Trust, Birmingham, UK (P.A.C., P.L., J.d.G.); University of Cambridge, Cambridge, UK (P.A.C.); Papworth Hospital National Health Service Foundation Trust, Cambridge, UK (P.A.C., B.S.R., L.M.S.); Sussex Cardiac Centre, Brighton and Sussex University Hospitals, Brighton, UK (J.C., D.W., D.H.-S.); Edinburgh Royal Infirmary, Edinburgh, UK (D.N.); The Heart Hospital, University College London, London, UK (M.J.M.); Imperial College Healthcare National Health Service Trust, London, UK (I.M.); University Hospitals Bristol National Health Service Foundation Trust, Bristol, UK (M.T.); Heart and Lung Centre, New Cross Hospital, Wolverhampton, UK (S.K.); University Hospital Southampton National Health Service Foundation Trust, Southampton, UK (G.R.V.); Walsgrave Hospital Coventry, Coventry, UK (M.B.); University Hospital North Staffordshire National Health Service Trust, Stoke-on-Trent, UK (R.B.); Leeds Teaching Hospitals National Health Service Trust, Leeds, UK (J.T.); King's College Hospital National Health Service Foundation Trust, London, UK (J.B., P.M.); Liverpool Heart and Chest Hospitals National Health Service Foundation Trust, Liverpool, UK (L.M.); and University Hospital of South Manchester, Manchester, UK (B.B.). david.hildick-smith@bsuh.nhs.uk.
Abstract
BACKGROUND: Postinfarction ventricular septal defect carries a grim prognosis. Surgical repair offers reasonable outcomes in patients who survive a healing phase. Percutaneous device implantation represents a potentially attractive early alternative. METHODS AND RESULTS: Postinfarction ventricular septal defect closure was attempted in 53 patients from 11 centers (1997-2012; aged 72±11 years; 42% female). Nineteen percent had previous surgical closure. Myocardial infarction was anterior (66%) or inferior (34%). Time from myocardial infarction to closure procedure was 13 (first and third quartiles, 5-54) days. Devices were successfully implanted in 89% of patients. Major immediate complications included procedural death (3.8%) and emergency cardiac surgery (7.5%). Immediate shunt reduction was graded as complete (23%), partial (62%), or none (15%). Median length of stay after the procedure was 5.0 (2.0-9.0) days. Fifty-eight percent survived to discharge and were followed up for 395 (63-1522) days, during which time 4 additional patients died (7.5%). Factors associated with death after postinfarction ventricular septal defect closure included the following: age (hazard ratio [HR]=1.04; P=0.039), female sex (HR=2.33; P=0.043), New York Heart Association class IV (HR=4.42; P=0.002), cardiogenic shock (HR=3.75; P=0.003), creatinine (HR=1.007; P=0.003), defect size (HR=1.09; P=0.026), inotropes (HR=4.18; P=0.005), and absence of revascularization therapy for presenting myocardial infarction (HR=3.28; P=0.009). Prior surgical closure (HR=0.12; P=0.040) and immediate shunt reduction (HR=0.49; P=0.037) were associated with survival. CONCLUSIONS: Percutaneous closure of postinfarction ventricular septal defect is a reasonably effective treatment for these extremely high-risk patients. Mortality remains high, but patients who survive to discharge do well in the longer term.
BACKGROUND: Postinfarction ventricular septal defect carries a grim prognosis. Surgical repair offers reasonable outcomes in patients who survive a healing phase. Percutaneous device implantation represents a potentially attractive early alternative. METHODS AND RESULTS: Postinfarction ventricular septal defect closure was attempted in 53 patients from 11 centers (1997-2012; aged 72±11 years; 42% female). Nineteen percent had previous surgical closure. Myocardial infarction was anterior (66%) or inferior (34%). Time from myocardial infarction to closure procedure was 13 (first and third quartiles, 5-54) days. Devices were successfully implanted in 89% of patients. Major immediate complications included procedural death (3.8%) and emergency cardiac surgery (7.5%). Immediate shunt reduction was graded as complete (23%), partial (62%), or none (15%). Median length of stay after the procedure was 5.0 (2.0-9.0) days. Fifty-eight percent survived to discharge and were followed up for 395 (63-1522) days, during which time 4 additional patients died (7.5%). Factors associated with death after postinfarction ventricular septal defect closure included the following: age (hazard ratio [HR]=1.04; P=0.039), female sex (HR=2.33; P=0.043), New York Heart Association class IV (HR=4.42; P=0.002), cardiogenic shock (HR=3.75; P=0.003), creatinine (HR=1.007; P=0.003), defect size (HR=1.09; P=0.026), inotropes (HR=4.18; P=0.005), and absence of revascularization therapy for presenting myocardial infarction (HR=3.28; P=0.009). Prior surgical closure (HR=0.12; P=0.040) and immediate shunt reduction (HR=0.49; P=0.037) were associated with survival. CONCLUSIONS: Percutaneous closure of postinfarction ventricular septal defect is a reasonably effective treatment for these extremely high-risk patients. Mortality remains high, but patients who survive to discharge do well in the longer term.
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